Tuesday, October 15, 2013

Indiana State to appeal high-fence deer hunting ruling

State to appeal high-fence deer hunting ruling

Oct. 15, 2013 3:12 PM
Indiana’s attorney general is going to appeal a recent court ruling that appears to open the door to more high-fence deer hunting in the state, and restrict the Department of Natural Resources’s authority to enforce state hunting laws on the private deer-hunting preserves.
Attorney General Greg Zoeller’s office filed notice of appeal today, two weeks after Harrison County Circuit Court Judge John Evans issued a ruling in favor of Rodney Bruce, who operates Whitetail Bluff, a preserve near Corydon.

In 2005 Bruce sued after the DNR tried to shut down his operation and the 11 other high-fence hunting preserves in the state at the time.

Owens ruling says that the DNR overstepped its authority, and that deer at facilities such as Bruce’s “are privately owned and not the property of the people of the state of Indiana,” so they’re not subject to the DNR’s oversight.

Evans’ ruling troubled animal rights activists and hunting groups who say they’re worried that it could severely restrict the ability of state wildlife officials to enforce state hunting laws inside the fenced enclosures, which they disparagingly call “canned hunts.” They say Evans ruling also challenged the notion that wildlife is owned by the public and only in special, tightly regulated circumstances can private individuals possess and kill the animals.

While the actual legal arguments behind the attorney general’s appeal haven’t yet been disclosed, both preserve operators and their critics hope the state appellate court clarifies the matter. Two judges have recently issued conflicting rulings on hunting preserves.

The Harrison County decision came 10 months after a judge in Owen County threw out a similar challenge by a preserve owner.
Call Star reporter Ryan Sabalow at (317) 444-6179. Follow him on Twitter:


Saturday, March 23, 2013
Rep. Matt Ubelhor of Bloomfield is going to amend Senate Bill 487 to include the legalization of “canned” deer hunting operations in Indiana ?
Tuesday, February 14, 2012
Oppose Indiana House Bill 1265 game farming cervids

Sunday, January 27, 2013

Indiana 6 deer missing from farm pose health risk to state herds

1/22/2013 11:11:00 AM

6 deer missing from farm pose health risk to state herds

Aubrey Woods, Tribune

Indiana Department of Natural Resourcescontinues to search for six ear-tagged deer in Jackson County and neighboring Bartholomew, Jennings and Scott counties. Those deer are among the 20 that escaped from a captive cervid facility — or deer farm — in 2012, a spokesman with the state Department of Natural Resources said Friday.

“Of the six, one is a buck, which had a yellow ear tag with the No. 47,” Phil Bloom said.

Bloom said the buck is the only one of the six missing deer imported from a site in Pennsylvania where deer have tested positive for chronic wasting disease.

“He has been exposed to it, but that doesn’t mean he has chronic wasting disease,” Bloom said. “There is no live test for chronic wasting disease. That can’t be determined until the deer is dead and tissue has been tested.”

Bloom said the other five deer that remain free are classified as exposed to chronic wasting disease through their association with the buck.

Of particular interest are any deer with a yellow ear tag bearing the prefix “IN 764” followed by another four numbers or any deer with a yellow ear tag and two numbers on it.

Natural Resources staff will assist in taking the deer carcass to Purdue University for testing at the Indiana Animal Disease Diagnostic Laboratory.

Of the remaining 20 that escaped from the deer farm, the owner recaptured 11 shortly after the escape.

The location and ownership of the deer farm have not been released, based on guidelines of the Indiana Board of Animal Health, but the owner is cooperating, Bloom said.

The escape occurred after a tree fell on a fence at the deer farm, Bloom said.

Of the remaining nine deer that escaped, one was struck and killed by a vehicle, a second was shot and killed by a bow hunter during archery season and a third was killed during a special deer hunting session the first weekend of January, Bloom said.

The owner of the farm continues to help search for the remaining six and has been cooperative with the state, Bloom said.

State officials believe the buck is still alive because people have reported seeing it, Bloom said.

“Although it is conceivable it may have been killed,” he said.

Hunters also may have killed some of the five missing deer and just not reported their deaths to the state as required, Bloom said.

Bloom said there are no special hunting seasons planned to find the remaining deer.

“We’re making an all-out effort to find the deer,” Bloom said.

Local hunter Chuck Brenner of Freetown said the state is being too complacent about an issue that could have long-range effects on the deer population, however.

“I’m not just a hunter,” Brenner said. “I’m a conservationist. We need to manage our herds.”

Brenner said chronic wasting disease could wipe out herds and cost the state millions of dollars down the road.

“We should hunt them down and find them whether it’s deer season or not,” Brenner said.

He said there hasn’t been much publicity about the missing deer and that local hunters could help with the search.

“They need to ask the local hunters for help,” Brenner said. “They could put out trail cameras. If nothing else, the state could put a bounty on them.”

Brenner said the deer are clearly marked and there could be a special hunt just for the six deer that are ear-tagged.

Bloom said the state wants to make sure that the deer are tracked down, tested and determined if they’ve been exposed to chronic wasting disease.

“It could have some far-reaching ramifications,” he said.

So far the disease has never been found in Indiana, which has been testing for the disease since 2002. More than 10,000 deer killed during hunts or by vehicles have been tested and the disease has not been detected, Bloom said.

The tags on those missing deer are expected to tell officials whether the animals have any possible connection with a captive facility in Pennsylvania where chronic wasting disease was confirmed this winter, Bloom said. That report made Pennsylvania the 23rd state in which it has been found.

Cervid or wild game farms in Indiana can raise deer, elk and moose for several reasons, Bloom said. The animals can be processed at a slaughterhouse and sold as meat, sold for pets or sold to high-fenced hunting reserves.

Copyright © 2013 The Tribune

Editor, John C. DePrez Jr.; Executive Editor, Carol Rogers; Publishers: IBRC and IAR

Long kills controversial fenced hunting bill

February 1, 2012 | Filed under: Issues,Top stories | Posted by: Lesley Weidenbener
By Lesley Weidenbener

The Statehouse File

INDIANAPOLIS – An effort to legalize fenced deer hunting is dead for this session. ...
see full text ;
Sunday, January 27, 2013
Indiana 6 deer missing from farm pose health risk to state herds INDIANA
how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ???



Tuesday, December 20, 2011




The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.


RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.






recently, a report came out in the U.K., about risk factors from entry of CWD from the USA. I think you might find interest there ;



Friday, December 14, 2012


DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012




In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.


Animals considered at high risk for CWD include:


1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and


2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.


Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.


The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.


Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.


There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.




36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.




The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).




In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.




In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.




Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.








Friday, December 14, 2012


DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012




Wednesday, September 25, 2013


Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE PRION 2013




DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability


Date: Fri, 16 May 2003 11:47:37 –0500


EMC 1 Terry S. Singeltary Sr. Vol #: 1









please see more on the potential of the prion uptake from plants, and see what SEAC said about the one study that showed prion uptake of the Tomato plant, although the test was never repeated ;



Furthermore, an unpublished study had indicated low level absorption of PrP from soil by tomato plants although it should be noted that this study had not been repeated. Details of this work would be sent to the SEAC Secretary. Dr Matthews explained that most of the manure from animals challenged with high doses of BSE had already been composted and used for coppicing. Members agreed that the risks from disposal of residual manure from experimental animals would be much less than historic risks of on farm contamination from naturally infected animals at the height of the BSE epidemic. ...SNIP...END


Uptake of Prions into Plants






Friday, August 09, 2013


***CWD TSE prion, plants, vegetables, and the potential for environmental contamination







Thursday, August 08, 2013


Characterization of the first case of naturally occurring chronic wasting disease in a captive red deer (Cervus elaphus) in North America




Sunday, September 01, 2013


hunting over gut piles and CWD TSE prion disease




Wednesday, September 04, 2013


***cwd - cervid captive livestock escapes, loose and on the run in the wild...




Saturday, June 29, 2013






Monday, June 24, 2013


The Effects of Chronic Wasting Disease on the Pennsylvania Cervid Industry Following its Discovery




Tuesday, June 11, 2013


CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania




Tuesday, May 28, 2013


Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013


6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.



Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Sheep Naturally/Experimentally Infected with Scrapie and Deer with Preclinical/Clinical Chronic Wasting Disease

  1. Richard Rubenstein1,*,
  2. Binggong Chang1,
  3. Perry Gray2,
  4. Martin Piltch2,
  5. Marie S. Bulgin3,
  6. Sharon Sorensen-Melson3 and
  7. Michael W. Miller4
+ Author Affiliations
  1. 1Departments of Neurology and Physiology/Pharmacology, SUNY Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, New York 11203
  2. 2Los Alamos National Laboratory, Los Alamos, New Mexico 87545
  3. 3University of Idaho, Caine Veterinary Teaching and Research Center, 1020 E. Homedale Road, Caldwell, Idaho 83607
  4. 4Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, Colorado 80526-2097


Prion diseases, also known as transmissible spongiform encephalopathies, are fatal neurodegenerative disorders. Low levels of infectious agent and limited, infrequent success of disease transmissibility and PrPSc detection have been reported with urine from experimentally infected clinical cervids and rodents. We report the detection of prion disease-associated seeding activity (PASA) in urine from naturally and orally infected sheep with clinical scrapie agent and orally infected preclinical and infected white-tailed deer with clinical chronic wasting disease (CWD). This is the first report on PASA detection of PrPSc from the urine of naturally or preclinical prion-diseased ovine or cervids. Detection was achieved by using the surround optical fiber immunoassay (SOFIA) to measure the products of limited serial protein misfolding cyclic amplification (sPMCA). Conversion of PrPC to PrPSc was not influenced by the presence of poly(A) during sPMCA or by the homogeneity of the PrP genotypes between the PrPC source and urine donor animals. Analysis of the sPMCA-SOFIA data resembled a linear, rather than an exponential, course. Compared to uninfected animals, there was a 2- to 4-log increase of proteinase K-sensitive, light chain immunoglobulin G (IgG) fragments in scrapie-infected sheep but not in infected CWD-infected deer. The higher-than-normal range of IgG levels found in the naturally and experimentally infected clinical scrapie-infected sheep were independent of their genotypes. Although analysis of urine samples throughout the course of infection would be necessary to determine the usefulness of altered IgG levels as a disease biomarker, detection of PrPSc from PASA in urine points to its potential value for antemortem diagnosis of prion diseases.


    • Received 13 May 2011.
    • Accepted 14 June 2011.
  • *Corresponding author. Mailing address: Downstate Medical Center, Departments of Neurology and Physiology/Pharmacology, Box 1213, 450 Clarkson Avenue, Brooklyn, NY 11203. Phone: (718) 270-2019. Fax: (718) 270-2459. E-mail: richard.rubenstein@downstate.edu.
  • Published ahead of print on 29 June 2011.







Thursday, June 09, 2011


Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission




Wednesday, March 18, 2009


Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay




doi:10.1016/j.febslet.2008.08.003 Copyright © 2008 Published by Elsevier B.V.


Detection of infectious prions in urine


Dennisse Gonzalez-Romeroa, Marcelo A. Barriaa, Patricia Leona, Rodrigo Moralesa and Claudio Soto, a,






Date: Sat, 20 Jul 2002 09:43:10 -0700

From: "Terry S. Singeltary Sr."


Date: Sat, 25 May 2002 18:41:46 -0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de

######## Bovine Spongiform Encephalopathy #########







now, what about those 'deer scents' of 100% urine', and the prion that is found in urine, why not just pass the prion with the urine to other deer...

Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urine collected at the peak of the rut, blended with Fresh Doe Urine for an extremely effective buck enticer. Use pre-rut before the does come into heat. Use during full rut when bucks are most active. Use during post-rut when bucks are still actively looking for does. 1 oz.




Works anytime of the year *

100 % Cow Elk-in-Heat urine (2oz.) *

Economical - mix with water in spray mist bottle *

Use wind to your advantage

Product Code WP-ESB $9.95


prions in urine?




Monday, June 17, 2013

Early detection of chronic wasting disease prions in urine of pre-symptomatic deer by real-time quaking-induced conversion assay




Tuesday, September 10, 2013


Review and Updates of the USDA-APHIS Veterinary Services (VS) National Chronice Wasting Disease (CWD) Program 2012-2013




Sunday, August 11, 2013


Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013


Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010




CWD transmission to humans.




never say never with the TSE prion.






Sunday, August 25, 2013


HD.13: CWD infection in the spleen of humanized transgenic mice


Liuting Qing and Qingzhong Kong


Case Western Reserve University; Cleveland, OH USA


Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals. ***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.


Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system


Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1


1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK


Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.


Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.


Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.


Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay. ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.






Sunday, August 25, 2013


***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission




Sunday, July 21, 2013


*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?




> sCJDMM1-2 should be considered as a separate entity at this time.


> All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.






*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.




now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????



“Our conclusion stating that we found no strong evidence of CWD transmission to humans”


From: TSS (216-119-163-189.ipset45.wt.net)




Date: September 30, 2002 at 7:06 am PST


From: "Belay, Ermias"




Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"


Sent: Monday, September 30, 2002 9:22 AM




Dear Sir/Madam,


In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.


That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.


Ermias Belay, M.D. Centers for Disease Control and Prevention



-----Original Message-----




Sent: Sunday, September 29, 2002 10:15 AM


To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV




Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS


Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease


2008 1: Vet Res. 2008 Apr 3;39(4):41


A prion disease of cervids: Chronic wasting disease


Sigurdson CJ.




*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,





full text ;






CJD REPORT 1994 increased risk for consumption of veal and venison and lamb






Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)



These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...


Table 9 presents the results of an analysis of these data.


There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).


Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.


There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).


The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).


There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).


The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).




It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).




In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...




In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)



snip...see full report ;




Thursday, October 10, 2013


CJD REPORT 1994 increased risk for consumption of veal and venison and lamb






October 1994


Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ


Dear Mr Elmhirst,




Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.


The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.


The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.


The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.


I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.





Tuesday, October 15, 2013


AD.47: Polymorphic variations in cervid prion protein affect CWD agent properties




Friday, April 26, 2013

INDIANA Republican State Sen. Travis Holdman Senate Bill 373 ag-gag WILL PUT HUMANS AT RISK



Saturday, September 21, 2013


Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT


FOR 4 YEARS, THE USDA NSLP fed our children all across the USA, from school to school, county to county, state to state, the most high rish cattle for mad cow type disease i.e. the TSE prion disease, they fed our children dead stock downer cows. did your children consume this, and will you have to wait 5 decades to see if they become exposed and go clinical with CJD TSE prion disease ???




Monday, September 02, 2013


Atypical BSE: role of the E211K prion polymorphism




Location: Virus and Prion Research Unit





Sunday, September 1, 2013


Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy


We previously described the biochemical similarities between PrPres derived from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations suggest a link between these two uncommon prion phenotypes in a primate model (it is to note that such a link has not been observed in other models less relevant from the human situation as hamsters or transgenic mice overexpressing ovine PrP [28]). We speculate that a group of related animal prion strains (L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion diseases in humans with a type 2 PrPres molecular signature (and more specifically type 2B for vCJD)




Together with previous experiments performed in ovinized and bovinized transgenic mice and hamsters [8,9] indicating similarities between TME and L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME outbreaks in North America and Europe during the mid-1900s.




Sunday, August 11, 2013

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010

Sunday, October 13, 2013

CJD TSE Prion Disease Cases in Texas by Year, 2003-2012

Sunday, October 13, 2013

Prion Disease Cases in Texas by Year, 2003-2012


Wednesday, October 09, 2013





Tuesday, September 24, 2013


NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)


Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15







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